Evidence map›Paper›PMID 33041976›Full record

ReviewFrontiers in neurology2020

Tuberous Sclerosis Complex as Disease Model for Investigating mTOR-Related Gliopathy During Epileptogenesis.

Till S Zimmer, Diede W M Broekaart, Victoria-Elisabeth Gruber, Erwin A van Vliet, Angelika Mühlebner, Eleonora Aronica

Abstract readReview
In one paragraph

Review in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Tuberous sclerosis complex.Nature reviews. Disease primers · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. mTOR Signaling: Recent Progress.International journal of molecular sciences · 2024
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Till S ZimmerDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Diede W M BroekaartDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Victoria-Elisabeth GruberDepartment of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
Erwin A van VlietDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Angelika MühlebnerDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.
Eleonora AronicaDepartment of (Neuro)Pathology, Amsterdam Neuroscience, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberous sclerosis complex (TSC) represents the prototypic monogenic disorder of the mammalian target of rapamycin (mTOR) pathway dysregulation. It provides the rational mechanistic basis of a direct link between gene mutation and brain pathology (structural and functional abnormalities) associated with a complex clinical phenotype including epilepsy, autism, and intellectual disability. So far, research conducted in TSC has been largely neuron-oriented. However, the neuropathological hallmarks of TSC and other malformations of cortical development also include major morphological and functional changes in glial cells involving astrocytes, oligodendrocytes, NG2 glia, and microglia. These cells and their interglial crosstalk may offer new insights into the common neurobiological mechanisms underlying epilepsy and the complex cognitive and behavioral comorbidities that are characteristic of the spectrum of mTOR-associated neurodevelopmental disorders. This review will focus on the role of glial dysfunction, the interaction between glia related to mTOR hyperactivity, and its contribution to epileptogenesis in TSC. Moreover, we will discuss how understanding glial abnormalities in TSC might give valuable insight into the pathophysiological mechanisms that could help to develop novel therapeutic approaches for TSC or other pathologies characterized by glial dysfunction and acquired mTOR hyperactivation.

Indexed as

astrocyteepilepsyepileptogenesisgliamammalian target of rapamycin (mTOR)microgliaoligodendrocytetuberous sclerosis (TSC)

Identifiers

PMID33041976
PMCPMC7527496

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.